Pulmonary

Front 1

What are 5 causes of hypoxemia?

Back 1

Shunt
V/Q mismatch
Diffusion abnormality
Alveolar hypoventilation
Reduced FiO2

Front 2

What are 3 causes of hypercapnia?

Back 2

Alveolar hypoventilation
Increased dead space ventilation
Increased CO2 production in setting of fixed ventilation

Front 3

Obstructive Disease Mnemonic

Back 3

Foreign body
Asthma
Chronic bronchitis + bronchiectasis
Emphysema
Small vessel disease

Front 4

Restrictive Disease Mnemonic

Back 4

Pleural
Alveolar filling
Interstitial lung
Neuromuscular
Thoracic cage

Front 5

What is the most common reason for hypoxemia in ILD?

Back 5

V/Q mismatch

Front 6

Broad-based budding and multiple nuclei

Back 6

Blastomycosis

Front 7

Pleomorphic yeast with mucinous capsule

Back 7

Cryptococcus

Front 8

Necrotizing granulomas with small yeast on silver or PAS

Back 8

Histoplasmosis

Front 9

Spherules with endospores

Back 9

Coccidiomycosis

Front 10

How does inflation of the lung effect blood flow?

Back 10

Alveolar vessels are compressed as lung expands
Extraalveolar vessels are pulled open by the lung parenchyma

Front 11

Transmural pressure of alveoli

Back 11

P_intravascular - P_alveolar

Front 12

Lung zones 1,2, and 3

Back 12

Zone 1: PA > Pa > Pv = DEAD SPACE
Zone 2: Pa > PA > Pv
Zone 3: Pa > Pv > PA

Front 13

Effect of high PACO2 and low pH on pulmonary vascular resistance

Back 13

Vasoconstriction but weaker than hypoxemia

Front 14

NO and Atrial natriueretic factor

Back 14

Relax pulmonary smooth muscle

Front 15

Prostaglandin I and platelet activating factor effect on pulm vascular tone

Back 15

Decrease

Front 16

Starling's law for pulmonary capillaries

Back 16

(P_cap - P_interstitial) - (Oncotic_cap - Oncotic_interstitial)

Front 17

Pulmonary arterial pressure equation

Back 17

Pa = PVR*CO + PCWP

Front 18

Causes of pulmonary hypertension (use equation) (3)

Back 18

Increased CO - left -> right shunts
Increased PVR - hypoxic vasoconstriction, tumor, inflammation
Increased PCWP - left ventricular disease (mitral stenosis)

Front 19

Fetal circulation shunts

Back 19

Ductus arteriosus - Pulmonary artery to aorta
Foramen ovale
Hypoxic vasoconstriction in utero is released at birth allowing flow through lungs

Front 20

Minute ventilation

Back 20

Respiratory rate X Tidal volume
Normal is 5-6 L/min

Front 21

Physiologic dead space equation

Back 21

VD/VT = (PaCO2 - PeCO2)/PaCO2

Usually = .3 ((40-28)/40)

Front 22

Pressure of oxygen starting from atm thru venous

Back 22

Atm - 160
Trachea - 150
Alveolus - 104
Arterial - 100
Venous - 40

Front 23

Factors regulating bronchial smooth muscle tone

Back 23

Parasympathetic - constriction
Sympathetic - dilation
Inflammatory mediators (leukotrienes, prostaglandins), chemical irritants, immediate hypersensitivity response (histamine) -> constriction

Front 24

Where is the majority of airway resistance?

Back 24

Large airways due to small total cross sectional area

Front 25

Collapsing tendency of lung is due to what 2 forces?

Back 25

Elastic recoil - 1/3
Surface tension - 2/3

Front 26

As radius decreased does surface tension get bigger or smaller?

Back 26

Bigger
P= 2T/r
More pressure is required to keep it from collapsing
Surface tension makes T vary with r so that P is constant and smaller alveoli dont collapse into larger

Front 27

Function residual capacity

Back 27

Relaxation volume.
Tendency for lung to recoil inward and for chest wall to spring outward is balance
Palv = Patm

Front 28

Factors that increase airways resistance

Back 28

Smooth muscle hypertrophy/hyperplasia
Abnormal smooth muscle contraction
Mucus gland/goblet cell hypertrophy
Excess mucus
Inflammatory cell infiltation
Edema of airway wall

Front 29

What causes hyperinflation?

Back 29

B/c of expiratory flow limitation, cannot expire all of air and is still expiring when have to take next breath. They increase lung volume so that the airways can stay open long enough to breathe

Front 30

Factors that decrease compliance (6)

Back 30

Fluid or air in pleural space
Thickening or fibrosis of pleural space
Flooded alveoli
Fibrotic interstitium
Infiltration of interstitium
Thoracic cage less mobile or more difficult to expand

Front 31

How is most O2 and CO2 transported in blood?

Back 31

O2 on hemoglobin
CO2 as bicarbonate

Front 32

Haldane effect

Back 32

Oxygenation of blood decreases the amount of CO2 bound to hemoglobin

Front 33

Causes of increased PaCO2 using the alveolar ventilation equation

Back 33

Decr minute ventilation (cant breathe due to muscle weakness or wont b/c of cns depression
Incr dead space
Incr VCO2 alone does not incr PaCO2 in health, only w/ underlying disease due to inability to increase minute vent

Front 34

Shunt vs dead space

Back 34

Shunt - perfusion w/o ventilation
Dead space - ventilation w/o pefusion

Front 35

Pulsus paradoxus

Back 35

Abnormally large decrease in systolic pressure upon inspiration

Front 36

Around what PaO2 is hemoglobin saturated?

Back 36

60 mmHg

Front 37

4 causes of v/q mismatch

Back 37

COPD
Pulmonary embolism
Pulmonary edema
Pneumonia

Front 38

Equation for carrying capacity of oxygen

Back 38

CaO2 = 1.34(Hgb)(SaO2) + .003(PO2)

Front 39

Equation for oxygen delivery

Back 39

DO2 = CaO2 X CO

Front 40

Classic sign for PAH

Back 40

Dyspnea on exertion

Front 41

Two explanations for reduced DLCO

Back 41

Membrane component - interstitial lung disease
Capillary component - pulmonary hypertension

Front 42

What makes sputum green?

Back 42

Neutrophils

Front 43

What is the mechanism for hypoxemia in COPD?

Back 43

V/Q mismatch due to airway disease

Front 44

Key criteria for ARDS (4)

Back 44

Bilateral infiltrates
PaO2/FiO2 < 100-200
Decreased compliance
No evidence of cardiogenic

Front 45

Effects of hyperinflation on diaphragm

Back 45

Fibers shorten and decrease force ->
Inability to increase ab pressure, paradoxical inward movement of abs on inspiration

Front 46

Consequences of respiratory muscle dysfunction (3)

Back 46

Hypoventilation
Aspiration (malfunction of upper airway muscles)
Impaired cough

Front 47

Dorsal respiratory group

Back 47

Inspiratory ramp signal cycling

Front 48

Ventral respiratory group (3)

Back 48

PreBotzinger complex - rhythm generator w/ pacemaker cells that excite DRG
Inspiratory neurons receive input from DRG
Expiratory neurons output to expiratory muscles for exercise

Front 49

Apneustic center

Back 49

Excitatory effect on VRG to prolong ramp action potentials
(triggered if a-pneu)

Front 50

Pneomotaxic center

Back 50

Switch off inspiration
(triggered if pneumo)

Front 51

Ventilatory response to hypercapnia

Back 51

Linear in the physiologic range of PaCO2
PO2 levels affect sensitivity of response of CO2 receptors so there is a stronger response to hypercapnia if hypoxemia is present

Front 52

Ventilatory response to hypoxemia

Back 52

Aortic and carotid bodies sense PO2 drops < 60 mmHg

Front 53

Central chemoreceptors

Back 53

Increased CO2 ->
CO2 crosses BBB ->
Elevated H+ detected in CSF

Front 54

Hering-Breuer Reflex

Back 54

Slowly adapting pulmonary stretch mechanoreceptors in tracheobronchial tree
Fire when lung volume increases
Sends signal via CN X to pneumotaxic center to terminate inspiration

Front 55

Rapidly adapting stretch receptors

Back 55

In upper airways
Respond to tissue distension and irritation
(cough)

Front 56

J receptors

Back 56

In alveoli and small conducting airways
Respond to interstitial edema and engorgement of pulm caps -> closure of larynx and apnea and rapid shallow breathing

Front 57

Apnea vs hypopnea and apnea-hypopnea index

Back 57

Apnea = complete lack of airflow for < 10 s
Hypopnea = airflow reduction of > 30% assoc w/ oxy desat of > 4%
AHI = #apneas+hypopnease / total sleep time
OSA = AHI >5

Front 58

Obstructive sleep apnea

Back 58

Central drive is working but upper airway collapse obstruct breathing during sleep

Front 59

Obesity-hyperventilation syndrome

Back 59

Progressive accumulation of CO2 over time and brainstem no longer response to hypercapnia

Front 60

OSA associated features (6)

Back 60

Depression
EDS
GERD
Impotence
Anxiety
Cognitive

Front 61

OSA treatment (3)

Back 61

Avoid alcohol, depressants
Weight loss
CPAP

Front 62

OHS (3)

Back 62

BMI > 30
Daytime PaCO2 > 45
No other causes
(mech = leptin resistance?)

Front 63

OHS presentation

Back 63

Sleepiness
Morning headaches
Mood
Dyspnea

Front 64

OHS treatment (2)

Back 64

Respiratory stim
Mechanical vent

Front 65

Albuterol (SE?)

Back 65

Short acting B2 agonist ->
Incr cAMP ->
Relaxes smooth muscle
B1 side effects: tachycardia, HTN
OSA: 10-20 min for 4-6 hr

Front 66

Salmeterol

Back 66

Long acting B2 agonist
Slow onset
Long duration

Front 67

Ipratropium

Back 67

Short acting anticholinergic (blocks muscarinic action)
More effective in COPD than asthma since more enhanced parasymp tone in COPD

Front 68

Tiotropium

Back 68

Long acting anticholinergic
Less affinity for M2 which is inhibitory for negative feedback so greater bronchodilatory effects

Front 69

Theophylline

Back 69

Methylxanthine phosphodiesterase inhibitor ->
Incr cAMP
Weak bronchodilators but might also be anti inflammatory, respiratory stimulant
CYP450 metabolism so lots of drug interactions

Front 70

Leukotriene antagonists

Back 70

Inhibiit 5-lipoxygenase or block LT receptors
Leukotrienes enhance inflammatory response and cause bronchoconstriction

Front 71

Inhaled corticosteroids

Back 71

Principally anti inflammatory but have lots of systemic SE: cataracts, osteoporosis, oral thrush from deposition in mouth

Front 72

Cromolyn

Back 72

Blocks release of histamine and leukotrienes from mast cells
For exercise-induced asthma and pediatrics

Front 73

Nedocromil

Back 73

Blocks release of mediators from eosinophils, macrophages, platelets, and mast cells

Front 74

Broncho vs lobar pneumonia

Back 74

Broncho is patchy distribution in terminal and resp bronchioloes
Lobar is diffuse uniform CONSOLIDATION of an entire lobe

Front 75

Stages of lobar pneumonia

Back 75

Congestion - vasc dilation and fluid accumulation in alv
Red hepatization - consolidated and red w/ vascular congestion and intra alv exudate (protein, RBC, PMNs)
Gray hepatization - firm lobe, bloodless septa and alv spaces filled w/ PMNs + fibrin
Resolution - enzymatic digestion of exudate and restoration of normal lung

Front 76

Gram positive diplococcus
Most common cause of CAP

Back 76

Strep pneumococcus

Front 77

Gram negative rod
Exacerbations of COPD

Back 77

H. influenzae

Front 78

Gram positive cocci
Infections in IVDA
Abscesses

Back 78

Staph aureus

Front 79

Gram negative rod
Alcoholics or debilitated patients

Back 79

Klebsiella

Front 80

Gram negative rod
CF or nosocomial
Invades blood vessels

Back 80

Pseudomonas pneumoniae

Front 81

Weakly gram negative rod
Lives in H2O reservoirs
Causes severe disease

Back 81

Legionella

Front 82

Aerobic gram positive rod
Filamenous
Acid fast red
In immunocompromised

Back 82

Nocardia

Front 83

Anaerobic gram negative
Filamentous
In normal hosts oral cavity
Acid fast neg

Back 83

Actinomyces

Front 84

Lung abscesses (what do they contain and what causes them?)

Back 84

Localized area of necrosis containing neutrophils
Aspiration of infective material, post infectious, septic emboli, tumors

Front 85

Mycobacterium avium intracellulare complex

Back 85

AIDS patients w/ CD4 < 60
Disseminated
Acid fast bacilli in macrophages
if AIDS - no granulomas
if no AIDS - caseating granulomas

Front 86

Emphysema (2)

Back 86

Abnormal permanent distal (to terminal non resp bronchiole) airspace enlargement
Destructive changes in alveolar wall w/o fibrosis
Smoking -> neutrophils -> proteases or ROS

Front 87

Centrilobular vs panlobular emphysema (common causes for each)

Back 87

Centri - respiratory bronchioloes only, upper lobes, most common in smokers
Pan - whole acinus, lower lobes, a1 anti trypsin

Front 88

Chronic bronchitis clinical diagnosis

Back 88

Clinical diagnosis:
Excess mucous
Cough most days for 3 mo for 2 years
Not necessary to have airflow obstruction

Front 89

3 mechanisms of COPD

Back 89

1. Chronic inflammation - neutrophil recruitment and CD8s
2. Proteinase/antiproteinase imbalance
3. Oxidative stress - free oxygen radicals

Front 90

Pathophys of COPD dyspnea (3)

Back 90

Increased WOB
Decreased diaphragm function
Hypoxemia - due to airway obstruction -> v/q mismatch

Front 91

Why is there hypercapnia in COPD?

Back 91

Increased dead space

Front 92

COPD treatment (4)

Back 92

Smoking cessation improves survival and O2 therapy if hypoxemic
Short acting bronchodilators for dyspnea
Long acting bronchodilators and ICS
Pulmonary rehab

Front 93

Bronchiectasis (definition and etiologies)

Back 93

Permanent abnormal dilatation and destruction of bronchial walls
Requires infectious insult plus impairment of drainage, airway obstruction, and/or defect in host defense

Front 94

Pathogenesis of cystic fibrosis lung disease

Back 94

Defective CFTR does not put Cl- into lumen, Na goes into cell and water follows leaving dry mucus ->
Infection and inflammation

Front 95

PFTs in CF and treatment

Back 95

Mixed
Airway toilet via chest PT
Antibiotics - inhaled tobimycin
DNase
B2 agonists NOT anticholinergics
(Pseudomonas infections may be lethal)

Front 96

Pathophys hallmarks of asthma (4)

Back 96

Airflow obstruction caused by bronchoconstriction
Airway edema
AHR
Airway remodeling

Front 97

Clinical hallmarks of asthma (3)

Back 97

Intermittent cough
Dyspnea
Wheezing

Front 98

Asthma pathogenesis (5)

Back 98

APC in airway epithelium bind allergen via IgE -> activate (overexpressed Th2 cells -> IL secretion -> eosinophil recruitment and mast cell activation -> AIRWAY INFLAMMATION

Front 99

Asthma: early vs late bronchospasm

Back 99

Early - 30 minutes, activated macrophages, cells release inflammatory mediators -> bronchospasm, vasodilation, edema, mucus secretion
Late - 4-6 hr, recruit and activation of eosinophils -> lots of cytokines and mediators -> AIRWAY INFLAMMATION, mucus secretion, edema, bronchoconstriction

Front 100

Asthma: causes of chest tightness and dyspnea

Back 100

Airflow obstruction (2/2 inflam, b/c, mucus, remodling) -> increased w.o.b, v/q mismatch, hyperinflation

Front 101

Asthma PFTs

Back 101

Obstructive but improve w/ BD
Normal DLCO
Lung volumes can be increased

Front 102

Asthma: 4 features of airway remodling

Back 102

Loss of ciliated epithelial cells and increase in mucus by goblets
Thickened BM
Fibroblast activation w/ collagen
Smooth muscle hyperresponsiveness and hypertrophy

Front 103

Asthma differential

Back 103

Children - foreign body asp, CF
Adults - GERD, postnasal drip, bronchiectasis, sarcoid, copd . . .

Front 104

Asthma treatment steps (5)

Back 104

SABA
ICS
ICS + LABA
ICS + LABA + LTM
Anti IgE

Front 105

Chronic bronchitis histology (4)

Back 105

Increased size and # of mucus glands
Increased Reid index
Goblet cell hyperplasia
Chronic inflammation

Front 106

Bronchiectasis gross and histo

Back 106

Dilated bronchi and bronchioles
Ulceration
Inflammation + fibrosis of bronchial wall
Squamous metaplasia

Front 107

ILD: Physiology (3 steps, O2 and CO2)

Back 107

Decreased compliance (due to fibrosis) ->
Increased w.o.b. ->
Decreased PaO2 (w/ exercise)
Hypercapnia as disease worsens b/c CO2 is more diffusible
V/Q mismatch

Front 108

What is major cause of hypoxemia in ILD

Back 108

V/Q mismatch

Front 109

ILD Radiology (two key findings)

Back 109

Diffuse bilateral infiltrates
"Ground glass" -> inflammation
Honeycomb -> fibrosis

Front 110

Smoking related ILDs (3)

Back 110

DIP, RB-ILD, Langerhans cell histiocytosis

Front 111

Pulmonary fibrosis complications (5)

Back 111

Respiratory failure
PE
Lung cancer
Pneumothorax
PH/cor pulmonale

Front 112

Cryptogenic organizing pneumonia (presentation, etiology, Rx)

Back 112

Pres: cough, dyspnea, weight loss, flu
Can be secondary or idiopathic
Rx: steroids

Front 113

Sarcoidosis (3 findings)

Back 113

Findings: enlarged hilar lymph
Well-formed non caseating non necrotizing granulomas
Eleveated ACE

Front 114

Diffuse alveolar hemorrhage (2 examples)

Back 114

Goodpasture's - anti GBM
Wegener's - c-ANCA
Both are systemic

Front 115

IFN-gamma vs TGF-beta

Back 115

IFN - proinflammatory and antifibrotic
TGF - profibrotic and antiinflammatory

Front 116

Hypersensitivity pneumonitis (granulomas?)

Back 116

Type III and IV (granuloma formation
CD8 proliferation
Chronic can progress to fibrosis

Front 117

UIP vs COP

Back 117

UIP - diffuse (also AIP)
COP - patchy (also sarcoid)

Front 118

Viral pneumonia histology

Back 118

Chronic interstitial infiltrate: lymphocytes, plasma cells, macrophages
DAD - hyaline membranes

Front 119

Fungal pneumonia infection histo

Back 119

Necrotizing granulomas w/ rim of histiocytes
Silver stains identify fungus

Front 120

Miss. river and bat droppings

Back 120

Histoplasmosis

Front 121

Waterways, Central US

Back 121

Blastomycosis

Front 122

Southwest US, Mexico

Back 122

Coccidiomycosis

Front 123

Cysts with black dot in center
Low CD4 count AIDS patients

Back 123

Pneumocystis jiroveci

Front 124

Aspergillosis (immunocompetent vs compromised)

Back 124

Competent - allergic bronchopulmonary aspergillosis (mucoid impaction of bronchi, eosinophils), fungus ball
Compromised - invasive

Front 125

If necrotizing granuloma in fungal pneumonia . . .

Back 125

Histoplasmosis
Coccidiomycosis
Blastomycosis

Front 126

Physiologic response to hypoxemic respiratory failure (type I)

Back 126

Increased catecholamines -> incr HR
Incr carotid body stim -> tachypnea -> incr vent

Front 127

Physiologic response to hypercapnic respiratory failure (type II)

Back 127

decr pH
incr ICP -> CO2 necrosis

Front 128

Physiologic adaptation to chronic resp failure (2)

Back 128

Incr erythropoietin -> incr hgb
Incr bicarbonate so less severe acidosis

Front 129

Causes of acute respiratory failure type I (6)

Back 129

anything that can cause shunt or v/q mismatch
ALI - ARDS
Pneumonia
Cardiogenic pulm edema
PE
Pneumothorax
Severe acute ILD

Front 130

Causes of acute resp failure type II (5)

Back 130

Drugs
Spinal cord injury
Acute neuromuscular disease (guillan barre, als)
COPD exacerabation
Status asthmaticus

Front 131

O2 therapy for acute vs chronic hypoexmia

Back 131

Acute - high flow high FiO2
Chronic - low flow, lower FiO2

Front 132

O2 therapy complications (3)

Back 132

Resorption atelectasis
Hypercapnia in COPD (due to incr dead space, haldane effecte)
ALI

Front 133

Indications for mechanical ventilation (3)

Back 133

Refractory hypoxemic respiratory failure: shunt, atelectasis
Ventilatory (hypercapnic) resp failure
Inability to protect airways

Front 134

NIV indications

Back 134

COPD exacerbations and immunocompromised hosts

Front 135

What causes resorption atelectasis in O2 therapy

Back 135

High concentration of O2 washes out NO which was helping to keep airways open

Front 136

3 things that cause hypercapnia in COPD when given O2 therapy

Back 136

1. O2 releases hyopemic vasoconstriction
2. Haldane effect
3. Abnormal respiratory drive means COPDers cant correct minute ventilation when VCO2 goes up

Front 137

Causes of ARDS

Back 137

Pulmonary - pneumonia, aspiration, inhalation, chest trauma
Extrapulmonary - sepsis, shock, trauma, transfusion

Front 138

ARDS pathophys (3 steps with 5 results)

Back 138

Acute lung injury ->
Increased permeability ->
Increased lung water in interstitium and alveoli ->
Decr compliance, shunt, hypoxemia, incr PA pressure from vasoconstriction, injured type II cells differentiate to type I

Front 139

Barotrauma, volutrauma, atelectrauma

Back 139

Barotrauma - air leaks into pleural space -> pneumothorax
Volutrauma - overdistension of alveoli -> release of mediators -> biotrauma
Atelectrauma - shearing force from constant opening and closing

Front 140

Granulomatous vasculitis with palisading histiocytes

Back 140

Wegener's granulomatosis

Front 141

Eosinophils, Birbeck granules

Back 141

Langerhans

Front 142

UIP path (3)

Back 142

Cobblestone pleura
Young = fibroblastic foci w/ spindle cells, Old = collagen

Front 143

COP path

Back 143

Collagen plugs of fibroplastic tissue elongated in bronchioles

Front 144

Acute interstitial pneumonia path

Back 144

DAD w/ hyaline membranes like ARDS

Front 145

DIP path

Back 145

(similar to RB-ILD)
Alveoli filled w/ pigmented macrophages
Not much fibrosis

Front 146

Alveoli filled w/ pigmented macrophages

Back 146

DIP

Front 147

Hypersensitivity pneumonitis path

Back 147

Lymphocytic infiltrates around bronchioles extending to alv septae
Poorly formed, non necrotizing granulomas

Front 148

Definition of pulmonary hypertension

Back 148

mean PA > 25 w/ PCWP < 15
If PCWP > 15, pulmonary venous hypertension

Front 149

How does hypoxia cause pulmonary hypertension?

Back 149

Vasoconstriction leading to remodeling of vessels and abnormal presence of smooth muscle (peripheralization)

Front 150

WHO PH groups

Back 150

I - idiopathic PAH and PAH in setting of conn tissue disease (scleroderma), HIV, cirrhosis, portal HTN . . .
2 - PVH from left heart disease
3 - From hypoxia (sleep apnea, OHS, high altitude) or parenchymal (COPD)
4- - Thromboembolic

Front 151

PH treatment (3)

Back 151

By pathogenesis:
Vasodilators (Ca blockers, endothelin antag, NO, prostacyclins, PDE5 inhibitors)
Oxygen
Anticoagulants

Front 152

Pathophys of PH (5)

Back 152

Endothelial injury ->
Increase in vasoconstrictors/decrease in vasodilators ->
Vasoconstriction ->
Remodeling w/ smooth muscle ->
In situ thrombosis

Front 153

Pulmonary embolism risk factors

Back 153

Virchow's triad:
Stasis
Inflammation
Hypercoagulability

Front 154

Pulmonary edema path

Back 154

Congested alv cap
Pink precipitate in alveolar spaces
Heart failure cells = macs w/ hemosiderin

Front 155

ARDS path: acute (5)

Back 155

Exudative
Edema
Hemorrhage
Hyaline membranes

Front 156

ARDS path: subacute (when and 2 features)

Back 156

7-10 days after injury
Type II replaced by type I
Fibroblasts in interstitium and alv spaes

Front 157

ARDS path: chronic (when and 2 features)

Back 157

2-3 wks
Fibrosis w/ architectural distortion
Cyst formation

Front 158

PAH histo (4)

Back 158

Medial hypertrophy
Intimal thickening
Muscularization of arterioles
Angiomatoid and plexiform lesions

Front 159

Pleura blood supply

Back 159

Visceral - arterial from bronchial systemic and venous to pulmonary (low pressure)
Parietal - arterial and venous both systemic (high pressure)

Front 160

Pleura lymphatics

Back 160

Visceral - not involved in clearage
Parietal - via stoma

Front 161

Pleura innervation

Back 161

Visceral - no sensory nerve endings
Parietal - richly innervated w/ sensory: costal and peripheral diaphragmatic via intercostal and central by phrenic for referred pain

Front 162

Identifying Exudate

Back 162

Pleural fluid protein/serum protein > .5
Pleural fluid LDH/serum LDH > .6

Front 163

Principle causes of transudative effusion (4)

Back 163

CHF -> RV failure/increased systemic - increased parietal, LV failure/increased venous - visceral pleura
Hepatic -> transdiaphragmatic flow
Nephrotic -> hypoalbuminemia
Atelectasis -> decreased pressure in pleural space

Front 164

Why is gas absorbed from pleural space?

Back 164

Because the sum of pressures in the venous blood in lower than the sum of pressure in the pleural space

Front 165

Principle causes of exudative effusion (4)

Back 165

Malignancy - disruption of mesothelium and caps
Inflammation
Chylothorax - lymphatic obstruction of parietal pleura somata
PE

Front 166

Parapneumonic vs empyema

Back 166

Parapneumonic - infection in adjacent lung -> pleural effusion
Empyema - infection in pleural space

Front 167

Pleural effusion treatment: trans vs exudate

Back 167

Transudate - underlying cuase
Exudate - can drain

Front 168

Pneuthorax presentation

Back 168

Acute onset of pleuritic chest pain and dyspnea
Tension
--> CHEST TUBE ASAP if large tension

Front 169

Pneumothorax types (4) and etiologies

Back 169

Primary - idiopathic, in tall thin young men secondary to subpleural blub
Secondary - w/ underlying lung disease: COPD, CF, astham . . .rupture of distended alveoli w/ leakage of air into interstitial then pleural space
Traumatic - penetrating wounds
Iatrogenic - visceral pleura punctured during invasive procedures

Front 170

Pneumothorax Rx

Back 170

If small, nothing or O2 to displace N2 in cap blood and reduce pressure so air goes into blood
If large, chest tube drainge or catheter aspiration

Front 171

Squamous cell carcinoma path (4)

Back 171

Central
Cavitate
Hypercalcemia
Keratin pearls

Front 172

Adenocarcinoma (3)

Back 172

Most common
Peripheral
(Broncheoalveolar adenocarc grows in septae and doesnt invade)

Front 173

Large cell lung cancer (2)

Back 173

Poorly differentiated
Central or peripheral

Front 174

Carcinoid

Back 174

Has neuroendocrine differentiation
Low grade malignancy
Can look like SCLC but w/ much fewer cells

Front 175

TTF-1 and CEA

Back 175

Adenocarcinoma

Front 176

Calretinin-1

Back 176

Mesothelioma

Front 177

Nasopharyngeal carcinoma

Back 177

Associated w/ EBV
Upper cervical lymphadenopathy

Front 178

Key radiographic features of malignancy (4)

Back 178

Increased size - > 2.5 cm
Ragged/spiculated margins
Double time is b/w 2wks and 200 days
Absence of calcification

Front 179

Equations for metabolic acidosis and alkalosis

Back 179

dPaCO2 = dHCO3 X 1.25 (acidosis)
dPaCO2 = dHCO3 X .6 (alkalosis)